Toll-like receptors and innate immunity

被引:347
作者
Uematsu, Satoshi
Akira, Shizuo
机构
[1] ERATO, Japan Sci & Technol Corp, Suita, Osaka 5650871, Japan
[2] Osaka Univ, Dept Host Def, Microbial Dis Res Inst, Suita, Osaka 5650851, Japan
来源
JOURNAL OF MOLECULAR MEDICINE-JMM | 2006年 / 84卷 / 09期
关键词
TLR; NLR; RIG-I;
D O I
10.1007/s00109-006-0084-y
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
The innate immune system is an evolutionally conserved host defense mechanism against pathogens. Innate immune responses are initiated by pattern recognition receptors (PRRs), which recognize specific structures of microorganisms. Among them, Toll-like receptors (TLRs) are capable of sensing organisms ranging from bacteria to fungi, protozoa, and viruses, and play a major role in innate immunity. However, TLRs recognize pathogens either on the cell surface or in the lysosome/endosome compartment. Recently, cytoplasmic PRRs have been identified to detect pathogens that have invaded cytosols. In this review, we focus on the functions of PRRs in innate immunity and their downstream signaling cascades.
引用
收藏
页码:712 / 725
页数:14
相关论文
共 120 条
[1]   The Crohn's disease protein, NOD2, requires RIP2 in order to induce ubiquitinylation of a novel site on NEMO [J].
Abbott, DW ;
Wilkins, A ;
Asara, JM ;
Cantley, LC .
CURRENT BIOLOGY, 2004, 14 (24) :2217-2227
[2]   Recognition of pathogen-associated molecular patterns by TLR family [J].
Akira, S ;
Hemmi, H .
IMMUNOLOGY LETTERS, 2003, 85 (02) :85-95
[3]   Toll receptor families: structure and function [J].
Akira, S .
SEMINARS IN IMMUNOLOGY, 2004, 16 (01) :1-2
[4]   Pathogen recognition and innate immunity [J].
Akira, S ;
Uematsu, S ;
Takeuchi, O .
CELL, 2006, 124 (04) :783-801
[5]   De novo CIAS1 mutations, cytokine activation, and evidence for genetic heterogeneity in patients with neonatal-onset multisystem inflammatory disease (NOMID) -: A new member of the expanding family of pyrin-associated autoinflammatory diseases [J].
Aksentijevich, I ;
Nowak, M ;
Mallah, M ;
Chae, JJ ;
Watford, WT ;
Hofmann, SR ;
Stein, L ;
Russo, R ;
Goldsmith, D ;
Dent, P ;
Rosenberg, HF ;
Austin, F ;
Remmers, EF ;
Balow, JE ;
Rosenzweig, S ;
Komarow, H ;
Shoham, NG ;
Wood, G ;
Jones, J ;
Mangra, N ;
Carrero, H ;
Adams, BS ;
Moore, TL ;
Schikler, K ;
Hoffman, H ;
Lovell, DJ ;
Lipnick, R ;
Barron, K ;
O'Shea, JJ ;
Kastner, DL ;
Goldbach-Mansky, R .
ARTHRITIS AND RHEUMATISM, 2002, 46 (12) :3340-3348
[6]   Hyporesponsiveness to vaccination with Borrelia burgdorferi OspA in humans and in TLR1- and TLR2-deficient mice [J].
Alexopoulou, L ;
Thomas, V ;
Schnare, M ;
Lobet, Y ;
Anguita, J ;
Schoen, RT ;
Medzhitov, R ;
Fikrig, E ;
Flavell, RA .
NATURE MEDICINE, 2002, 8 (08) :878-884
[7]   Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3 [J].
Alexopoulou, L ;
Holt, AC ;
Medzhitov, R ;
Flavell, RA .
NATURE, 2001, 413 (6857) :732-738
[8]   Evasion of Toll-like receptor 5 by flagellated bacteria [J].
Andersen-Nissen, E ;
Smith, KD ;
Strobe, KL ;
Barrett, SLR ;
Cookson, BT ;
Logan, SM ;
Aderem, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (26) :9247-9252
[9]   The V proteins of paramyxoviruses bind the IFN-inducible RNA helicase, mda-5, and inhibit its activation of the IFN-β promoter [J].
Andrejeva, J ;
Childs, KS ;
Young, DF ;
Carlos, TS ;
Stock, N ;
Goodbourn, S ;
Randall, RE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (49) :17264-17269
[10]   Hemagglutinin protein of wild-type measles virus activates Toll-like receptor 2 signaling [J].
Bieback, K ;
Lien, E ;
Klagge, IM ;
Avota, E ;
Schneider-Schaulies, J ;
Duprex, WP ;
Wagner, H ;
Kirschning, CJ ;
ter Meulen, V ;
Schneider-Schaulies, S .
JOURNAL OF VIROLOGY, 2002, 76 (17) :8729-8736